Deficiency in tumor necrosis factor alpha activity does not impair early protective Th1 responses against blood-stage malaria

Blood-stage Plasmodium chabaudi AS infection was controlled by 4 weeks in m ice with deletion of tumor necrosis factor p55 and p75 receptors (TNFR-knoc kout [KO]) and control wild-type (WT) mice, although female TNFR-KO mice sh owed slightly but significantly higher parasitemia immediately following th e peak Serum interleukin 12 (IL-12) p70 and gamma interferon (IFN-gamma) le vels were similar but tumor necrosis factor alpha levels were significantly higher in TNFR-KO mice than in Wr controls. Splenic IL-12 receptor beta(1) and beta 2 and IFN-gamma mRNA expression, as well as spleen cell productio n of IFN-gamma and IL 4, were comparable in both mouse types, but IL-10 pro duction was significantly higher in cells from TNFR-KO mice than in cells f rom WT mice. Lipopolysaccharide-induced NO secretion by splenic macrophages in vitro was significantly reduced but systemic NO3- levels were similar i n infected TNFR-KO and WT mice.